TSH,
temperature, pulse rate, and other indicators in hypothyroidism
A R T I C L E

TSH,
temperature, pulse rate, and other indicators in hypothyroidism

Each
of the indicators of thyroid function can be useful, but has to be interpreted
in relation to the physiological state.

Increasingly,
TSH (the pituitary thyroid stimulating hormone) has been treated as
if it meant something independently; however, it can be brought down
into the normal range, or lower, by substances other than the thyroid
hormones.

“Basal”
body temperature is influenced by many things besides thyroid. The resting
heart rate helps to interpret the temperature. In a cool environment,
the temperature of the extremities is sometimes a better indicator than
the oral or eardrum temperature.

The
“basal” metabolic rate, especially if the rate of carbon dioxide
production is measured, is very useful. The amount of water and calories
disposed of in a day can give a rough idea of the metabolic rate.

The
T wave on the electrocardiogram, and the relaxation rate on the Achilles
reflex test are useful.

Blood
tests for cholesterol, albumin, glucose, sodium, lactate, total thyroxine
and total T3 are useful to know, because they help to evaluate the present
thyroid status, and sometimes they can suggest ways to correct the problem.

Less
common blood or urine tests (adrenaline, cortisol, ammonium, free fatty
acids), if they are available, can help to understand compensatory reactions
to hypothyroidism.

A
book such as McGavack's The Thyroid, that provides traditional
medical knowledge about thyroid physiology, can help to dispel some
of the current dogmas about the thyroid.

Using
more physiologically relevant methods to diagnose hypothyroidism will
contribute to understanding its role in many problems now considered
to be unrelated to the thyroid.

======================================

I
have spoken to several people who told me that their doctors had diagnosed
them as “both hypothyroid and hyperthyroid.” Although physicists
can believe in things which are simultaneously both particles and not
particles, I think biology (and medicine, as far as it is biologically
based) should occupy a world in which things are not simultaneously
themselves and their opposites. Those illogical, impossible diagnoses
make it clear that the rules for interpreting test results have in some
situations lost touch with reality.

Until
the 1940s, hypothyroidism was diagnosed on the basis of signs and symptoms,
and sometimes the measurement of oxygen consumption (“basal metabolic
rate”) was used for confirmation. Besides the introduction of supposedly
“scientific” blood tests, such as the measurement of protein-bound
iodine (PBI) in the blood, there were other motives for becoming parsimonious
with the diagnosis of hypothyroidism. With the introduction of synthetic
thyroxine, one of the arguments for increasing its sale was that natural
Armour thyroid (which was precisely standardized by biological tests)
wasn't properly standardized, and that an overdose could be fatal. A
few articles in prestigious journals created a myth of the danger of
thyroid, and the synthetic thyroxine was (falsely) said to be precisely
standardized, and to be without the dangers of the complete glandular
extract.

Between
1940 and about 1950, the estimated percentage of hypothyroid Americans
went from 30% or 40% to 5%, on the basis of the PBI test, and it has
stayed close to that lower number (many publications claim it to be
only 1% or 2%). By the time that the measurement of PBI was shown to
be only vaguely related to thyroid hormonal function, it had been in
use long enough for a new generation of physicians to be taught to disregard
the older ideas about diagnosing and treating hypothyroidism. They were
taught to inform their patients that the traditional symptoms that were
identified as hypothyroidism before 1950 were the result of the patients'
own behavior (sloth and gluttony, for example, which produced fatigue,
obesity, and heart disease), or that the problems were imaginary (women's
hormonal and neurological problems, especially), or that they were simply
mysterious diseases and defects (recurring infections, arthritis, and
cancer, for example).

As
the newer, more direct tests became available, their meaning was defined
in terms of the statistical expectation of hypothyroidism that had become
an integral part of medical culture. To make the new TSH measurements
fit the medical doctrine, an 8- or 10-fold variation in the hormone
was defined as “normal.” With any other biological measurement,
such as erythrocyte count, blood pressure, body weight, or serum sodium,
calcium, chloride, or glucose, a variation of ten or 20 percent from
the mean is considered to be meaningful. If the doctrine regarding the
5% prevalence of hypothyroidism hadn't been so firmly established, there
would have been more interest in establishing the meaning of these great
variations in TSH.

In
recent years the “normal range” for TSH has been decreasing. In
2003, the American Association of Clinical Endocrinologists changed
their guidelines for the normal range to 0.3 to 3.0 microIU/ml. But
even though this lower range is less arbitrary than the older standards,
it still isn't based on an understanding of the physiological meaning
of TSH.

Over
a period of several years, I never saw a person whose TSH was over 2
microIU/ml who was comfortably healthy, and I formed the impression
that the normal, or healthy, quantity was probably something less than
1.0.

If
a pathologically high TSH is defined as normal, its role in major diseases,
such as breast cancer, mastalgia, MS, fibrotic diseases, and epilepsy,
will simply be ignored. Even if the possibility is considered, the use
of an irrational norm, instead of a proper comparison, such as the statistical
difference between the mean TSH levels of cases and controls, leads
to denial of an association between hypothyroidism and important diseases,
despite evidence that indicates an association.

Some
critics have said that most physicians are “treating the TSH,” rather
than the patient. If TSH is itself pathogenic, because of its pro-inflammatory
actions, then that approach isn't entirely useless, even when they “treat
the TSH” with only thyroxine, which often isn't well converted into
the active triiodothyronine, T3. But the relief of a few symptoms in
a small percentage of the population is serving to blind the medical
world to the real possibilities of thyroid therapy.

TSH
has direct actions on many cell types other than the thyroid, and probably
contributes directly to edema (Wheatley and Edwards, 1983), fibrosis,
and mastocytosis. If people are concerned about the effects of a TSH
“deficiency,” then I think they have to explain the remarkable longevity
of the animals lacking pituitaries in W.D. Denckla's experiments, or
of the naturally pituitary deficient dwarf mice that lack TSH, prolactin,
and growth hormone, but live about a year longer than normal mice (Heiman,
et al., 2003). Until there is evidence that very low TSH is somehow
harmful, there is no basis for setting a lower limit to the normal range.

Some
types of thyroid cancer can usually be controlled by keeping TSH completely
suppressed. Since TSH produces reactions in cells as different as fibroblasts
and fat cells, pigment cells in the skin, mast cells and bone marrow
cells (Whetsell, et al., 1999), it won't be surprising if it turns out
to have a role in the development of a variety of cancers, including
melanoma.

Many
things, including the liver and the senses, regulate the function of
the thyroid system, and the pituitary is just one of the factors affecting
the synthesis and secretion of the thyroid hormones.

A
few people who had extremely low levels of pituitary hormones, and were
told that they must take several hormone supplements for the rest of
their life, began producing normal amounts of those hormones within
a few days of eating more protein and fruit. Their endocrinologist
described them as, effectively, having no pituitary gland. Extreme malnutrition
in Africa has been described as creating “. . . a condition resembling
hypophysectomy,” (Ingenbleek and Beckers, 1975) but the people I talked
to in Oregon were just following what they thought were healthful nutritional
policies, avoiding eggs and sugars, and eating soy products.

Occasionally,
a small supplement of thyroid in addition to a good diet is needed to
quickly escape from the stress-induced “hypophysectomized” condition.

Aging,
infection, trauma, prolonged cortisol excess, somatostatin, dopamine
or L-dopa, adrenaline (sometimes; Mannisto, et al., 1979), amphetamine,
caffeine and fever can lower TSH, apart from the effect of feedback
by the thyroid hormones, creating a situation in which TSH can appear
normal or low, at the same time that there is a real hypothyroidism.

A
disease or its treatment can obscure the presence of hypothyroidism.
Parkinson's disease is a clear example of this. (Garcia-Moreno and Chacon,
2002: “... in the same way hypothyroidism can simulate Parkinson's
disease, the latter can also conceal hypothyroidism.”)

The
stress-induced suppression of TSH and other pituitary hormones is reminiscent
of the protective inhibition that occurs in individual nerve fibers
during dangerously intense stress, and might involve such a “parabiotic”
process in the nerves of the hypothalamus or other brain region. The
relative disappearance of the pituitary hormones when the organism is
in very good condition (for example, the suppression of ACTH and cortisol
by sugar or pregnenolone) is parallel to the high energy quiescence
of individual nerve fibers.

These
associations between energy state and cellular activity can be used
for evaluating the thyroid state, as in measuring nerve and muscle reaction
times and relaxation rates. For example, relaxation which is retarded,
because of slow restoration of the energy needed for cellular “repolarization,”
is the basis for the traditional use of the Achilles tendon reflex relaxation
test for diagnosing hypothyroidism. The speed of relaxation of the heart
muscle also indicates thyroid status (Mohr-Kahaly, et al., 1996).

Stress,
besides suppressing the TSH, acts in other ways to suppress the real
thyroid function. Cortisol, for example, inhibits the conversion of
T4 to T3, which is responsible for the respiratory production of energy
and carbon dioxide. Adrenaline, besides leading to increased production
of cortisol, is lipolytic, releasing the fatty acids which, if they
are polyunsaturated, inhibit the production and transport of thyroid
hormone, and also interfere directly with the respiratory functions
of the mitochondria. Adrenaline decreases the conversion to T4 to T3,
and increases the formation of the antagonistic reverse T3 (Nauman,
et al., 1980, 1984).

During
the night, at the time adrenaline and free fatty acids are at their
highest, TSH usually reaches its peak. TSH itself can produce
lipolysis, raising the level of circulating free fatty acids. This suggests
that a high level of TSH could sometimes contribute to functional hypothyroidism,
because of the antimetabolic effects of the unsaturated fatty acids.

These
are the basic reasons for thinking that the TSH tests should be given
only moderate weight in interpreting thyroid function.

The
metabolic rate is very closely related to thyroid hormone function,
but defining it and measuring it have to be done with awareness of its
complexity.

The
basal metabolic rate that was commonly used in the 1930s for diagnosing
thyroid disorders was usually a measurement of the rate of oxygen consumption,
made while lying quietly early in the morning without having eaten anything
for several hours. When carbon dioxide production can be measured at
the same time as oxygen consumption, it's possible to estimate the proportion
of energy that is being derived from glucose, rather than fat or protein,
since oxidation of glucose produces more carbon dioxide than oxidation
of fat does. Glucose oxidation is efficient, and suggests a state of
low stress.

The
very high adrenaline that sometimes occurs in hypothyroidism will increase
the metabolic rate in several ways, but it tends to increase the oxidation
of fat. If the production of carbon dioxide is measured, the adrenaline/stress
component of metabolism will be minimized in the measurement. When polyunsaturated
fats are mobilized, their spontaneous peroxidation consumes some oxygen,
without producing any usable energy or carbon dioxide, so this is another
reason that the production of carbon dioxide is a very good indicator
of thyroid hormone activity. The measurement of oxygen consumption was
usually done for two minutes, and carbon dioxide production could be
accurately measured in a similarly short time. Even a measurement of
the percentage of carbon dioxide at the end of a single breath can give
an indication of the stress-free, thyroid hormone stimulated rate of
metabolism (it should approach five or six percent of the expired air).

Increasingly
in the last several years, people who have many of the standard symptoms
of hypothyroidism have told me that they are hyperthyroid, and that
they have to decide whether to have surgery or radiation to destroy
their thyroid gland. They have told me that their symptoms of “hyperthyroidism,”
according to their physicians, were fatigue, weakness, irritability,
poor memory, and insomnia.

They
didn't eat very much. They didn't sweat noticeably, and they drank a
moderate amount of fluids. Their pulse rates and body temperature were
normal, or a little low.

Simply
on the basis of some laboratory tests, they were going to have their
thyroid gland destroyed. But on the basis of all of the traditional
ways of judging thyroid function, they were hypothyroid.

Broda
Barnes, who worked mostly in Fort Collins, Colorado, argued that the
body temperature, measured before getting out of bed in the morning,
was the best basis for diagnosing thyroid function.

Fort
Collins, at a high altitude, has a cool climate most of the year. The
altitude itself helps the thyroid to function normally. For example,
one study (Savourey, et al., 1998) showed an 18% increase in T3
at a high altitude, and mitochondria become more numerous and are more
efficient at preventing lactic acid production, capillary leakiness,
etc.

In
Eugene during a hot and humid summer, I saw several obviously hypothyroid
people whose temperature seemed perfectly normal, euthyroid by Barnes'
standards. But I noticed that their pulse rates were, in several cases,
very low. It takes very little metabolic energy to keep the body at
98.6 degrees when the air temperature is in the nineties. In cooler
weather, I began asking people whether they used electric blankets,
and ignored their temperature measurements if they did.

The
combination of pulse rate and temperature is much better than either
one alone. I happened to see two people whose resting pulse rates were
chronically extremely high, despite their hypothyroid symptoms. When
they took a thyroid supplement, their pulse rates came down to normal.
(Healthy and intelligent groups of people have been found to have an
average resting pulse rate of 85/minute, while less healthy groups average
close to 70/minute.)

The
speed of the pulse is partly determined by adrenaline, and many hypothyroid
people compensate with very high adrenaline production. Knowing that
hypothyroid people are susceptible to hypoglycemia, and that hypoglycemia
increases adrenaline, I found that many people had normal (and sometimes
faster than average) pulse rates when they woke up in the morning, and
when they got hungry. Salt, which helps to maintain blood sugar, also
tends to lower adrenalin, and hypothyroid people often lose salt too
easily in their urine and sweat. Measuring the pulse rate before and
after breakfast, and in the afternoon, can give a good impression of
the variations in adrenalin. (The blood pressure, too, will show the
effects of adrenaline in hypothyroid people. Hypothyroidism is a major
cause of hypertension.)

But
hypoglycemia also tends to decrease the conversion of T4 to T3, so heat
production often decreases when a person is hungry. First, their fingers,
toes, and nose will get cold, because adrenalin, or adrenergic sympathetic
nervous activity, will increase to keep the brain and heart at a normal
temperature, by reducing circulation to the skin and extremities. Despite
the temperature-regulating effect of adrenalin, the reduced heat production
resulting from decreased T3 will make a person susceptible to hypothermia
if the environment is cool.

Since
food, especially carbohydrate and protein, will increase blood sugar
and T3 production, eating is “thermogenic,” and the oral (or eardrum)
temperature is likely to rise after eating.

Blood
sugar falls at night, and the body relies on the glucose stored in the
liver as glycogen for energy, and hypothyroid people store very little
sugar. As a result, adrenalin and cortisol begin to rise almost as soon
as a person goes to bed, and in hypothyroid people, they rise very high,
with the adrenalin usually peaking around 1 or 2 A.M., and the cortisol
peaking around dawn; the high cortisol raises blood sugar as morning
approaches, and allows adrenalin to decline. Some people wake up during
the adrenalin peak with a pounding heart, and have trouble getting back
to sleep unless they eat something.

If
the night-time stress is very high, the adrenalin will still be high
until breakfast, increasing both temperature and pulse rate. The cortisol
stimulates the breakdown of muscle tissue and its conversion to energy,
so it is thermogenic, for some of the same reasons that food is thermogenic.

After
eating breakfast, the cortisol (and adrenalin, if it stayed high despite
the increased cortisol) will start returning to a more normal, lower
level, as the blood sugar is sustained by food, instead of by the stress
hormones. In some hypothyroid people, this is a good time to measure
the temperature and pulse rate. In a normal person, both temperature
and pulse rate rise after breakfast, but in very hypothyroid people
either, or both, might fall.

Some
hypothyroid people have a very slow pulse, apparently because they aren't
compensating with a large production of adrenalin. When they eat, the
liver's increased production of T3 is likely to increase both their
temperature and their pulse rate.

By
watching the temperature and pulse rate at different times of day, especially
before and after meals, it's possible to separate some of the effects
of stress from the thyroid-dependent, relatively “basal” metabolic
rate. When beginning to take a thyroid supplement, it's important to
keep a chart of these measurements for at least two weeks, since that's
roughly the half-life of thyroxine in the body. When the body has accumulated
a steady level of the hormones, and begun to function more fully, the
factors such as adrenaline that have been chronically distorted to compensate
for hypothyroidism will have begun to normalize, and the early effects
of the supplementary thyroid will in many cases seem to disappear, with
heart rate and temperature declining. The daily dose of thyroid often
has to be increased several times, as the state of stress and the adrenaline
and cortisol production decrease.

Counting
calories achieves approximately the same thing as measuring oxygen consumption,
and is something that will allow people to evaluate the various thyroid
tests they may be given by their doctor. Although food intake and metabolic
rate vary from day to day, an approximate calorie count for several
days can often make it clear that a diagnosis of hyperthyroidism is
mistaken. If a person is eating only about 1800 calories per day, and
has a steady and normal body weight, any “hyperthyroidism” is strictly
metaphysical, or as they say, “clinical.”

When
the humidity and temperature are normal, a person evaporates about a
liter of water for every 1000 calories metabolized. Eating 2000 calories
per day, a normal person will take in about four liters of liquid, and
form about two liters of urine. A hyperthyroid person will invisibly
lose several quarts of water in a day, and a hypothyroid person may
evaporate a quart or less.

When
cells, because of a low metabolic rate, don't easily return to their
thoroughly energized state after they have been stimulated, they tend
to take up water, or, in the case of blood vessels, to become excessively
permeable. Fatigued muscles swell noticeably, and chronically fatigued
nerves can swell enough to cause them to be compressed by the surrounding
connective tissues. The energy and hydration state of cells can be detected
in various ways, including magnetic resonance, and electrical impedance,
but functional tests are easy and practical.

With
suitable measuring instruments, the effects of hypothyroidism can be
seen as slowed conduction along nerves, and slowed recovery and readiness
for new responses. Slow reaction time is associated with slowed memory,
perception, and other mental processes. Some of these nervous deficits
can be remedied slightly just by raising the core temperature and providing
suitable nutrients, but the active thyroid hormone, T3 is mainly responsible
for maintaining the temperature, the nutrients, and the intracellular
respiratory energy production.

In
nerves, as in other cells, the ability to rest and repair themselves
increases with the proper level of thyroid hormone. In some cells, the
energized stability produced by the thyroid hormones prevents inflammation
or an immunological hyperactivity. In the 1950s, shortly after it was
identified as a distinct substance, T3 was found to be anti-inflammatory,
and both T4 and T3 have a variety of anti-inflammatory actions, besides
the suppression of the pro-inflammatory TSH.

Because
the actions of T3 can be inhibited by many factors, including polyunsaturated
fatty acids, reverse T3, and excess thyroxine, the absolute level of
T3 can't be used by itself for diagnosis. “Free T3” or “free T4”
is a laboratory concept, and the biological activity of T3 doesn't necessarily
correspond to its “freedom” in the test. T3 bound to its transport
proteins can be demonstrated to enter cells, mitochondria, and nuclei.
Transthyretin, which carries both vitamin A and thyroid hormones, is
sharply decreased by stress, and should probably be regularly measured
as part of the thyroid examination.

When
T3 is metabolically active, lactic acid won't be produced unnecessarily,
so the measurement of lactate in the blood is a useful test for interpreting
thyroid function. Cholesterol is used rapidly under the influence of
T3, and ever since the 1930s it has been clear that serum cholesterol
rises in hypothyroidism, and is very useful diagnostically. Sodium,
magnesium, calcium, potassium, creatinine, albumin, glucose, and other
components of the serum are regulated by the thyroid hormones, and can
be used along with the various functional tests for evaluating thyroid
function.

Stereotypes
are important. When a very thin person with high blood pressure visits
a doctor, hypothyroidism isn't likely to be considered; even high TSH
and very low T4 and T3 are likely to be ignored, because of the stereotypes.
(And if those tests were in the healthy range, the person would be at
risk for the “hyperthyroid” diagnosis.) But remembering some of
the common adaptive reactions to a thyroid deficiency, the catabolic
effects of high cortisol and the circulatory disturbance caused by high
adrenaline should lead to doing some of the appropriate tests, instead
of treating the person's hypertension and “under nourished” condition.

Rev Neurol (Paris). 1992;148(5):371-3. [Hashimoto's encephalopathy:
toxic or autoimmune mechanism?] [Article in French] Ghawche F, Bordet
R, Destee A. Service de Clinique Neurologique A, CHU, Lille. A 36-year-old
woman presented with partial complex status epilepticus. Magnetic resonance
imaging with T2-weighted sequences showed a high-intensity signal in
the left posterior frontal area. Hashimoto's thyroiditis was then discovered.
The disappearance of the high-intensity signal after corticosteroid
therapy was suggestive of an autoimmune mechanism. However, improvement
could be obtained only with a hormonal treatment, which supports the
hypothesis of a pathogenetic role of the Tyrosine-Releasing Hormone
(TRH).

Am J Clin Nutr. 1986 Mar;43(3):406-13. Thyroid hormone and carrier
protein interrelationships in children recovering rom kwashiorkor.
Kalk WJ, Hofman KJ, Smit AM, van Drimmelen M, van der Walt LA, Moore
RE. We have studied 15 infants with severe protein energy malnutrition
(PEM) as a model of nutritional nonthyroidal illness. Changes in circulating
thyroid hormones, binding proteins, and their interrelationships were
assessed before and during recovery. Serum concentrations of total thyroxine
and triiodothyronine and of thyroxine-binding proteins were extremely
reduced, and increased progressively during 3 wk of refeeding. The T4:TBG
molar ratio was initially 0.180 +/- 0.020, and increased progressively,
parallel to the increases in TT4, to 0.344 +/- 0.038 after 21 days (p
less than 0.025). The changes in free T4 estimates varied according
to the methods used--FTI and analogue FT4 increased, dialysis FT4 fraction
decreased. Serum TSH levels increased transiently during recovery. It
is concluded 1) there is reduced binding of T4 and T3 to TBG in untreated
PEM which takes 2-3 wk to recover; 2) there are methodological differences
in evaluating free T4 levels in PEM; 3) increased
TSH secretion appears to be an integral part of the recovery from PEM.

Neuroendocrinology. 1982;35(2):139-47.
Neurotransmitter control of thyrotropin secretion.
Krulich L. “The central dopaminergic system seems to have an inhibitory
influence on the secretion of thyrotropin (TSH) both in humans and rats.”

Rev
Neurol. 2002 Oct 16-31;35(8):741-2. [Hypothyroidism concealed by
Parkinson's disease][in Spanish] Garcia-Moreno JM, Chacon J. Servicio
de Neurologia, Hospital Universitario Virgen Macarena, Sevilla, Espana.
Sinue@arrakis.es AIMS: Although it is commonly recognised that diseases
of the thyroids can simulate extrapyramidal disorders, a review of the
causes of Parkinsonism in the neurology literature shows that they are
not usually mentioned or, if so, only very briefly. The development
of hypothyroidism in a patient with Parkinson s disease can go undetected,
since the course of both diseases can involve similar clinical features.
Generally speaking there is always an insistence on the need to conduct
a thyroidal hormone study in any patient with symptoms of Parkinson,
but no emphasis is put on the need to continue to rule out dysthyroidism
throughout the natural course of the disease, in spite of the fact that
the concurrence of both pathological conditions can be high and that,
in the same way hypothyroidism can simulate Parkinson s disease, the
latter can also conceal hypothyroidism. CASE REPORT: We report the case
of a female patient who had been suffering from Parkinson s disease
for 17 years and started to present on off fluctuations that did not
respond to therapy. Hypothyroidism was observed and the hormone replacement
therapy used to resolve the problem allowed the Parkinsonian fluctuations
to be controlled. CONCLUSIONS: We believe that it is very wise to suspect
hypothyroidism in patients known to be suffering from Parkinson s disease,
and especially so in cases where the clinical condition worsens and
symptoms no longer respond properly to antiparkinsonian treatment. These
observations stress the possible role played by thyroid hormones in
dopaminergic metabolism and vice versa.

Rev Neurol (Paris). 1985;141(1):55-8. [Hashimoto's thyroiditis and
myoclonic encephalopathy. Pathogenic hypothesis] [Article in French]
Latinville D, Bernardi O, Cougoule JP, Bioulac B, Henry P, Loiseau P,
Mauriac L. A 49 year old caucasian female with Hashimoto thyroiditis,
developed during two years a neurological disorder with tonic-clonic
and myoclonic seizures and confusional states. Some attacks were followed
by a transient postictal aphasia. Some parallelism was noted between
the clinical state and TSH levels. Neurological events disappeared
with the normalisation of thyroid functions. This association of Hashimoto
thyroiditis and myoclonic encephalopathy has been rarely published.
Pathogenesis could be double. Focal signs could be due to an auto-immune
mechanism, perhaps through a vasculitis. A non-endocrine central action
could explain diffuse signs: tonic-clonic seizures, myoclonus and confusional
episodes.

Epilepsy Res. 1988 Mar-Apr;2(2):102-10. Evidence of hypothyroidism
in the genetically epilepsy-prone rat. Mills SA, Savage DD. Department
of Pharmacology, University of New Mexico School of Medicine, Albuquerque
87131. A number of neurochemical and behavioral similarities exist between
the genetically epilepsy-prone (GEPR) rat and rats made hypothyroid
at birth. These similarities include lower brain monoamine levels, audiogenic
seizure susceptibility and lowered electroconvulsive shock seizure threshold.
Given these similarities, thyroid hormone status was examined in GEPR
rats. Serum samples were collected from GEPR-9 and non-epileptic control
rats at 5, 9, 13, 16, 22, 31, 45, 60, 90, 150 and 350 days of age. Serum
thyroxine (T4) levels were significantly lower in GEPR-9 rats compared
to control until day 22 of age. GEPR-9 thyrotropin (TSH) levels were
significantly elevated during the period of diminished serum T4. GEPR-9
triiodothyronine (T3) levels were lower than control throughout the
first year of life. The data indicate that the GEPR-9 rat is hypothyroid
from at least the second week of life up to 1 year of age. The critical
impact of neonatal hypothyroidism on brain function coupled with the
development of the audiogenic seizure susceptible trait by the GEPR-9
rat during the third week after birth suggests that neonatal hypothyroidism
could be one etiological factor in the development of the seizure-prone
state of GEPR-9 rats.

Przegl Lek. 1998;55(5):250-8. [Mastopathy and simple goiter--mutual
relationships] [Article in Polish] Mizia-Stec K, Zych F, Widala
E. “Non-toxic goitre was found in 80% patients with mastopathy,
and the results of palpation examination of thyroid were confirmed by
thyroid ultrasonographic examination. Non-toxic goitre was significantly
more often in patients with mastopathy in comparison with healthy women,
and there was found significantly higher thyroid volume in these patients.”
Endocrinology. 1997 Apr;138(4):1434-9. Thyroxine administration prevents
streptococcal cell wall-induced inflammatory responses. Rittenhouse
PA, Redei E.

Natl Med J India. 1998 Mar-Apr;11(2):62-5. Neuropsychological impairment
and altered thyroid hormone levels in epilepsy. Thomas SV, Alexander
A, Padmanabhan V, Sankara Sarma P. Department of Neurology, Sree Chitra
Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram,
Kerala, India. BACKGROUND: Neuropsychological impairment is a common
problem in epilepsy which interferes with the quality of life of patients.
Similarly, thyroid hormone levels have been observed to be abnormal
in patients with epilepsy on various treatments. This study aimed to
ascertain any possible correlation between neuropsychological performance
and thyroid hormone levels among epilepsy patients. METHODS: Thyroid
hormone levels, indices of neuropsychological performance and social
adaptation of 43 epilepsy patients were compared with those of age-
and sex-matched healthy control subjects. RESULTS: Epilepsy patients
exhibited significantly (p < 0.001) lower scores on attention, memory,
constructional praxis, finger tapping time, and verbal intelligence
quotient (i.q.) when compared with controls. Their
T3, T4 and Free T3 levels were significantly lower;
and TSH and Free T4 levels were significantly higher than that of
controls. There was no statistically significant correlation between
the indices of neuropsychological performance and thyroid hormone levels.
CONCLUSION: We did not observe any correlation between neuropsychological
impairment and thyroid hormone levels among patients with epilepsy.